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首页> 外文期刊>The Southeast Asian journal of tropical medicine and public health >ISONIAZID (INH) TREATMENT OF INH-RESISTANT MYCOBACTER1UM TUBERCULOSIS INHIBITS INFECTED MACROPHAGE TO-PRGDUcE TNF-alpha
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ISONIAZID (INH) TREATMENT OF INH-RESISTANT MYCOBACTER1UM TUBERCULOSIS INHIBITS INFECTED MACROPHAGE TO-PRGDUcE TNF-alpha

机译：异烟肼（INH）治疗抗INH的结核分枝杆菌会抑制感染巨噬细胞转胎TNF-α

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摘要

Macrophages undergo apoptosis after infected by Mycobacterium tuberculosis (M.tb), which is regulated by tumor necrosis factor alpha (TNF-alpha) and has a direct correlation with killing of intracellular bacilli. In order to clarify the role of isoniazid (INH) in the modulation of macrophages apoptosis and intracellular bacilli replication, we performed the following studies using an INH-resistant clinical M.tb isolate (INHres). Macrophages derived from peripheral blood were infected with INHres and treated or not treated with INH. Apoptosis was measured using an Ag-capture ELISA for histone and fragmented DNA. Production of TNF-a by INHres infected was assayed using ELISA and viability of intracellular M.tb was determined using bacterial culture of macrophage lysates on Lowenstein-Jensen (LJ) medium. INH pre-treatment to INHres reduced macrophages apoptosis, production of TNF-a and intracellular INHres viability. This study indicated that INH affected TNF-a release resulting in reduction of the extent macrophages apoptosis and of intracellular INH-resistant M.tb viability.
机译：巨噬细胞受结核分枝杆菌（M.tb）感染后会发生凋亡，这受肿瘤坏死因子α（TNF-alpha）调节，并与杀灭细胞内细菌有直接关系。为了阐明异烟肼（INH）在巨噬细胞凋亡和细胞内细菌复制调控​​中的作用，我们使用耐INH的临床M.tb分离株（INHres）进行了以下研究。来自外周血的巨噬细胞被INHres感染，并已用或未用INH治疗。使用Ag捕获ELISA测定组蛋白和片段化DNA的凋亡。使用ELISA分析感染的INHres产生的TNF-α，并通过在Lowenstein-Jensen（LJ）培养基上进行巨噬细胞裂解物的细菌培养来测定细胞内M.tb的活力。对INHres进行INH预处理可减少巨噬细胞凋亡，TNF-α的产生和细胞内INHres的活力。这项研究表明，INH影响TNF-a的释放，导致巨噬细胞凋亡程度的降低和细胞内INH耐药M.tb活力的降低。

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